- 【Updated on May 12, 2025】 Integration of CiNii Dissertations and CiNii Books into CiNii Research
- Trial version of CiNii Research Automatic Translation feature is available on CiNii Labs
- Suspension and deletion of data provided by Nikkei BP
- Regarding the recording of “Research Data” and “Evidence Data”
The Lipopolysaccharide-Induced Up-Regulation of Bradykinin B2-Receptor in the Mouse Heart Is Mediated by Tumor Necrosis Factor-.ALPHA. and Angiotensin II
-
- Yayama Katsutoshi
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
-
- Hiyoshi Hiromi
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
-
- Sugiyama Kaori
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
-
- Okamoto Hiroshi
- Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
Bibliographic Information
- Other Title
-
- The Lipopolysaccharide-Induced Up-Regulation of Bradykinin B2-Receptor in the Mouse Heart Is Mediated by Tumor Necrosis Factor-α and Angiotensin 2
- Lipopolysaccharide Induced Up Regulation of Bradykinin B2 Receptor in the Mouse Heart Is Mediated by Tumor Necrosis Factor アルファ and Angiotensin 2
Search this article
Description
Our present study aimed to characterize the effects of lipopolysaccharide (LPS) on the expression of the bradykinin B2-receptor in the mouse heart, which may have a role in cardiac depression during sepsis. We found that LPS induced the up-regulation of B2-receptor mRNA in the heart in vivo and in cultured cardiac myocytes in vitro. Like LPS, tumor necrosis factor-α (TNF-α) but not interleukin (IL)-1-β, IL-6 or endothelin-1 stimulated B2-receptor expression in cultured myocytes. The effect of LPS on the expression of B2-receptor mRNA was also mimicked in cardiac myocytes by Ang II via Ang II type 1 (AT1-) receptor. Losartan, an AT1-receptor antagonist, inhibited about 50% of the LPS-induced up-regulation of B2-receptor mRNA in the heart in vivo and in cultured cardiac myocytes in vitro. Furthermore, the up-regulation of B2-receptor mRNA by either LPS or Ang II in cultured myocytes was abolished by anti-TNF-α antibody. These results suggest that the up-regulation of cardiac B2-receptor expression by LPS is mediated through TNF-α, which is produced in the myocardium by two different mechanisms in an AT1-receptor-dependent and independent manners, implying the role of the cardiac kallikrein-kinin system in the development of cardiac dysfunction during sepsis.
Journal
-
- Biological and Pharmaceutical Bulletin
-
Biological and Pharmaceutical Bulletin 29 (6), 1143-1147, 2006
The Pharmaceutical Society of Japan
- Tweet
Keywords
Details 詳細情報について
-
- CRID
- 1390282679604214912
-
- NII Article ID
- 110005602257
-
- NII Book ID
- AA10885497
-
- ISSN
- 13475215
- 09186158
-
- NDL BIB ID
- 7921376
-
- PubMed
- 16755007
-
- Text Lang
- en
-
- Data Source
-
- JaLC
- NDL Search
- Crossref
- CiNii Articles
- OpenAIRE
-
- Abstract License Flag
- Disallowed